Effects of Celecoxib and Acetaminophen in Fracture Healing in Dogs : Current School News

Comparative Studies of the Effects of Celecoxib and Acetaminophen in Fracture Healing in Dogs

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Comparative Studies of the Effects of Celecoxib and Acetaminophen in Fracture Healing in Dogs.

ABSTRACT  

Fifteen dogs of similar age (8-12 months) were used for the clinical study. They were randomized into 3 groups (CH1-5, CL1-5 AND AC1-5). Simple transverse femoral fractures were created under anaesthesia using a bone saw. Spatial alignment of the bone was achieved by insertion of an intramedullary pin. Radiographic assessment confirmed that the pins were intact and internal fixation was thorough.

Celecoxib (Celebrex® Pfizer Inc, Germany) was supplied in encapsulated powdered form and was suspended in 0.5% dimethylsulphoxide (weight per volume) in sterile deionized water. Each dog in group 1 (CL1-5) was given 5mg/kg Celebrex®, group 2 (CH1-5) 10mg/kg Celebrex® and group3 (AC1-5) 20mg/kg acetaminophen (Divamol®, NDF Pharmaceuticals Ltd, Nigeria) orally three times daily.

Drug administration was commenced four hours after the creation of the fracture and was continued daily for the specified number of times for each study groups for two weeks. Sequential radiographs were taken to evaluate fracture healing at week 2, 4, 6, and 8 after surgery. Follow-up radiographs were compared with earlier radiographs to assess the dynamics of fracture healing.

Radiographic studies showed that fracture healing was not affected in dogs treated with 5mg/kg (Celebrex®), delayed union was observed in dogs treated with 10mg/kg (Celebrex®) and there was relatively high incidence of nonunion in dogs treated with acetaminophen. Celebrex® at a dose of 5mg/kg did not affect fracture callus formation and did not cause a significant increase in the proportion of delayed union fracture. 

INTRODUCTION   

A major component of post-operative pain is induced by peripheral and central sensitization of structures involved in nociception. This leads to an exaggerated response to noxious stimuli (hyperalgesia), a spread of hypersensitivity to non-injured tissue (secondary hypergesia), and a reduction in intensity of stimuli necessary to initiate pain (allodynia). Pain can be minimized by use of analgesic drugs prior to pain stimulation, such as surgery.

Benefits of pre-emptive analgesia have been demonstrated for opioids and ketoprofen (Vuolteenaho et al, 2008, Delong et al, 1999, Helfet et al, 1999). Non-steroidal anti-inflammatory drugs (NSAIDs) are some of the most widely used analgesics for the treatment of acute postoperative and post-traumatic pain (Wolfe et al, 1999, Kendall and Peura, 1993). They also have been extensively used to alleviate chronic pain and discomfort associated with osteoarthritis (Dubois et al, 1998).

The primary mode of action of this class of compounds is the inhibition of cyclooxygenase (COX) activity leading to a reduction in prostaglandin production and its effects on both inflammation and pain (McAdam et al, 1999, Davies et al, 1984). The COX enzyme family is encoded by two genes COX-1 and COX-2. Each of these genes encodes several isotopic variants that arise by differential splicing (Vane and Botting, 1997, Huntjens et al, 2005).

The first generation of drugs developed, the non-steroidal anti-inflammatory drugs, inhibit the activities of both COX enzymes; however, their use has been associated with prolonged bleeding time and gastric irritation, sometimes leading to ulceration. Subsequent research demonstrated that COX-1 was expressed in many tissues and that two of its primary x functions are the protection of gastric mucosa and the regulation of platelet aggregation (Roos and Simmons 2005, Lipsky et al, 2000). 

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CSN Team.

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